北方稻田生态系统研究Ⅱ．稻萍结合系统细绿萍共生固N量研究

对稻萍结合系统细绿萍共生固Ｎ量研究表明,萍的固Ｎ力在整个生长季不同时期有所变化．最高固Ｎ率出现在６月初,萍固Ｎ量随其接种量和水稻行距增加而增加．５０～１０ｃｍ宽窄行交替的水稻行距和１５００ｋｇ·ｈｍ－２的萍接种量的稻萍结合系统的总固Ｎ量为１０７．１ｋｇ·ｈｍ－２,而３０ｃｍ等行距的３２５ｋｇ·ｈｍ－２的萍接种量的稻－萍结合系统的总固Ｎ量仅为３６．０ｋｇ·ｈｍ－２     

中药远志的研究进展

对近年来远志的资源、商品、鉴别、化学成分、药理活性及栽培方面进行了系统的综述,并就商品远志在市场上存在的问题及发展前景进行了探讨。     

Detection and validation of a small broad-host-range plasmid pBBR1MCS-2 for use in genetic manipulation of the extremely acidophilic Acidithiobacillus sp

An efficient genetic system for introducing genes into biomining microorganisms is essential not only to experimentally determine the functions of genes predicted based on bioinformatic analysis, but also for their genetic breeding. In this study, a small broad-host-range vector named pBBR1MCS-2, which does not belong to the IncQ, IncW, or IncP groups, was studied for the feasibility of its use in conjugative gene transfer into extremely acidophilic strains of Acidithiobacillus. To do this, a recombinant plasmid pBBR-tac-Sm, a derivative of pBBR1MCS-2, was constructed and the streptomycin resistant gene (Sm(r)) was used as the reporter gene. Using conjugation, pBBR-tac-Sm was successfully transferred into three tested strains of Acidithiobacillus. Then we measured its transfer frequency, its stability in Acidithiobacillus cells, and the level of resistance to streptomycin of the transconjugants and compared this with the IncQ plasmid pJRD215 control. Our results indicate that pBBR1MCS-2 provides a new and useful tool in the genetic manipulation of Acidithiobacillus strains.     

Calcitonin gene-related peptide promotes proliferation and inhibits apoptosis in endothelial progenitor cells via inhibiting MAPK signaling

Background

Calcitonin gene-related peptide (CGRP) contributes to bone formation by stimulating bone marrow stromal cell (BMSC) proliferation and differentiation. However, the proliferative and apoptotic effects of CGRP on bone marrow-derived endothelial progenitor cells (EPCs) have not been investigated.

Methods

We tested the effects of CGRP on EPC proliferation and apoptosis by Cell Counting Kit-8, flow cytometry, and studied the effects of CGRP on the expression of proliferation- and apoptosis-related markers in EPCs and the underlying mitogen-activated protein kinase (MAPK) signalling pathway by quantitative polymerase chain reaction and western blotting.

Results

We detected EPC markers (CD34, CD133 and VEGFR-2) in 7-day cultures and found that CGRP (10^??10–10^??12 M) promoted the proliferation of cultured EPCs, with a peak increase of 30% at 10^??10 M CGRP. CGRP also upregulated the expression of proliferation-associated genes, including cyclin D1 and cyclin E, and increased the percentages of G2/M-phase and S-phase cells after incubation 72 h. CGRP inhibited serum deprivation (SD)-induced apoptosis in EPCs after 24 and 48 h and downregulated the expression of apoptosis-related genes, including caspase-3, caspase-8, caspase-9 and Bax. Phosphorylated (p-)ERK1/2, p-p38 and p-JNK protein levels in EPCs treated with CGRP were significantly lower than those in untreated EPCs. Pre-treatment with the calcitonin receptor-like receptor (CRLR) antagonist CGRP8–37 or a MAPK pathway inhibitor (PD98059, SB203580 or SP600125) completely or partially reversed the pro-proliferative and anti-apoptotic effects and the reduced p-ERK1/2, p-p38 and p-JNK expression induced by CGRP.

Conclusion

Our results show that CGRP exerts pro-proliferative and anti-apoptotic effects on EPCs and may act by inhibiting MAPK pathways.

     

Interruption of intrachromosomal looping by CCCTC binding factor decoy proteins abrogates genomic imprinting of human insulin-like growth factor II

Monoallelic expression of IGF2 is regulated by CCCTC binding factor (CTCF) binding to the imprinting control region (ICR) on the maternal allele, with subsequent formation of an intrachromosomal loop to the promoter region. The N-terminal domain of CTCF interacts with SUZ12, part of the polycomb repressive complex-2 (PRC2), to silence the maternal allele. We synthesized decoy CTCF proteins, fusing the CTCF deoxyribonucleic acid-binding zinc finger domain to CpG methyltransferase Sss1 or to enhanced green fluorescent protein. In normal human fibroblasts and breast cancer MCF7 cell lines, the CTCF decoy proteins bound to the unmethylated ICR and to the IGF2 promoter region but did not interact with SUZ12. EZH2, another part of PRC2, was unable to methylate histone H3-K27 in the IGF2 promoter region, resulting in reactivation of the imprinted allele. The intrachromosomal loop between the maternal ICR and the IGF2 promoters was not observed when IGF2 imprinting was lost. CTCF epigenetically governs allelic gene expression of IGF2 by orchestrating chromatin loop structures involving PRC2.     

Tracing the origin and evolution of plant TIR-encoding genes

Toll-interleukin-1 receptor (TIR)-encoding proteins represent one of the most important families of disease resistance genes in plants. Studies that have explored the functional details of these genes tended to focus on only a few limited groups; the origin and evolutionary history of these genes were therefore unclear. In this study, focusing on the four principal groups of TIR-encoding genes, we conducted an extensive genome-wide survey of 32 fully sequenced plant genomes and Expressed Sequence Tags (ESTs) from the gymnosperm Pinus taeda and explored the origins and evolution of these genes. Through the identification of the TIR-encoding genes, the analysis of chromosome positions, the identification and analysis of conserved motifs, and sequence alignment and phylogenetic reconstruction, our results showed that the genes of the TIR-X family (TXs) had an earlier origin and a wider distribution than the genes from the other three groups. TIR-encoding genes experienced large-scale gene duplications during evolution. A skeleton motif pattern of the TIR domain was present in all spermatophytes, and the genes with this skeleton pattern exhibited a conserved and independent evolutionary history in all spermatophytes, including monocots, that followed their gymnosperm origin. This study used comparative genomics to explore the origin and evolutionary history of the four main groups of TIR-encoding genes. Additionally, we unraveled the mechanism behind the uneven distribution of TIR-encoding genes in dicots and monocots.     

A FAK scaffold inhibitor disrupts FAK and VEGFR-3 signaling and blocks melanoma growth by targeting both tumor and endothelial cells

Melanoma has the highest mortality rate of all skin cancers and a major cause of treatment failure is drug resistance. Tumors heterogeneity requires novel therapeutic strategies and new drugs targeting multiple pathways. One of the new approaches is targeting the scaffolding function of tumor related proteins such as focal adhesion kinase (FAK). FAK is overexpressed in most solid tumors and is involved in multiple protein-protein interactions critical for tumor cell survival, tumor neovascularization, progression and metastasis. In this study, we investigated the anticancer activity of the FAK scaffold inhibitor C4, targeted to the FAK-VEGFR-3 complex, against melanomas. We compared C4 inhibitory effects in BRAF mutant vs BRAF wild type melanomas. C4 effectively caused melanoma tumor regression in vivo, when administered alone and sensitized tumors to chemotherapy. The most dramatic effect of C4 was related to reduction of vasculature of both BRAF wild type and V600E mutant xenograft tumors. The in vivo effects of C4 were assessed in xenograft models using non-invasive multimodality imaging in conjunction with histologic and molecular biology methods. C4 inhibited cell viability, adhesion and motility of melanoma and endothelial cells, specifically blocked phosphorylation of VEGFR-3 and FAK and disrupted their complexes. Specificity of in vivo effects for C4 were confirmed by a decrease in tumor FAK and VEGFR-3 phosphorylation, reduction of vasculogenesis and reduced blood flow. Our collective observations provide evidence that a small molecule inhibitor targeted to the FAK protein-protein interaction site successfully inhibits melanoma growth through dual targeting of tumor and endothelial cells and is effective against both BRAF wild type and mutant melanomas.     

两种杀虫剂对稻田捕食性天敌集团捕食功能的影响

将稻田各类捕食性天敌作为一集团,运用功能法评价了甲胺磷和杀虫双对该集团捕食功能的影响,由于各类捕食性天敌对杀虫剂敏感性的不同,甲胺磷和杀虫双造成的各类天敌的死亡率和残存天敌个体的捕食功能减退率均不同。实验表明,隐翅虫类和狼蛛类对甲胺磷较为敏感,而对杀虫双,肖蛸类最为敏感。杀虫双对隐翅虫类的致死作用及捕食功能影响较小。就集团的捕食功能而言,甲胺磷影响明显大于杀虫双,但在总的功能减退率组分中,甲胺磷致     

江西高天岩自然保护区生态系统服务功能价值评估

高天岩自然保护区位于江西省莲花县,为当地人提供了多项生态服务功能。根据高天岩自然保护区生态与社会经济系统的特征,构建其生态系统服务功能价值评估指标体系,并以2014年数据为基础,综合运用成本替代、市场价值、影子工程、造林成本、成果参数和旅行费用等定量分析方法,评估其生态系统的经济价值。结果表明:2014年,高天岩自然保护区生态系统服务总经济价值为7.20×10~8元,其中,土壤保持和固碳释氧的经济价值居前两位,分别为4.39×10~8元和1.16×10~8元,各占服务总经济价值的60.89%和16.11%。9项服务指标按评估的经济价值大小排序为:土壤保持固碳释氧产品供给生物多样性保护环境净化气候调节旅游休憩调洪蓄水社会保障。直观的经济数字反映了高天岩自然保护区生态系统对人类社会的重要贡献,一方面有利于强化管理者和公众保护高天岩自然保护区的意识,另一方面为政府制定高天岩自然保护区生态系统补偿标准提供数据支撑。